中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2015年
3期
377-379
,共3页
郭培培%吴会生%严虹%陈璟莉%袁世荧
郭培培%吳會生%嚴虹%陳璟莉%袁世熒
곽배배%오회생%엄홍%진경리%원세형
右美托咪啶%再灌注损伤%脑%氧化性应激
右美託咪啶%再灌註損傷%腦%氧化性應激
우미탁미정%재관주손상%뇌%양화성응격
Dexmedetomidine%Reperfusion injury%Brain%Oxidative stress
目的 评价右美托咪定对大鼠全脑缺血再灌注时氧化应激反应的影响.方法 健康雄性SD大鼠36只,体重250~ 300 g,采用随机数字表法分为3组(n=12):假手术组(S组)、全脑缺血再灌注组(I/R组)和右美托咪定组(D组).采用夹闭双侧颈总动脉联合低血压法制备大鼠全脑缺血再灌注损伤模型.D组于再灌注即刻经颈总静脉注射右美托咪定3 μg/kg负荷剂量,随后以3 μg· kg-1·h-1的速率静脉输注至再灌注2h.于再灌注24 h时行神经功能缺陷评分(NDS评分),然后处死大鼠,取脑组织,计数凋亡细胞,计算细胞凋亡率,测定丙二醛(MDA)、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的水平.结果 与S组比较,I/R组和D组NDS评分、细胞凋亡率和MDA水平升高,SOD和CAT的水平降低(P<0.01);与I/R组比较,D组NDS评分、细胞凋亡率和MDA水平降低,SOD和CAT的水平升高(P<0.01).结论 右美托咪定通过抑制氧化应激反应减轻大鼠全脑缺血再灌注损伤.
目的 評價右美託咪定對大鼠全腦缺血再灌註時氧化應激反應的影響.方法 健康雄性SD大鼠36隻,體重250~ 300 g,採用隨機數字錶法分為3組(n=12):假手術組(S組)、全腦缺血再灌註組(I/R組)和右美託咪定組(D組).採用夾閉雙側頸總動脈聯閤低血壓法製備大鼠全腦缺血再灌註損傷模型.D組于再灌註即刻經頸總靜脈註射右美託咪定3 μg/kg負荷劑量,隨後以3 μg· kg-1·h-1的速率靜脈輸註至再灌註2h.于再灌註24 h時行神經功能缺陷評分(NDS評分),然後處死大鼠,取腦組織,計數凋亡細胞,計算細胞凋亡率,測定丙二醛(MDA)、超氧化物歧化酶(SOD)和過氧化氫酶(CAT)的水平.結果 與S組比較,I/R組和D組NDS評分、細胞凋亡率和MDA水平升高,SOD和CAT的水平降低(P<0.01);與I/R組比較,D組NDS評分、細胞凋亡率和MDA水平降低,SOD和CAT的水平升高(P<0.01).結論 右美託咪定通過抑製氧化應激反應減輕大鼠全腦缺血再灌註損傷.
목적 평개우미탁미정대대서전뇌결혈재관주시양화응격반응적영향.방법 건강웅성SD대서36지,체중250~ 300 g,채용수궤수자표법분위3조(n=12):가수술조(S조)、전뇌결혈재관주조(I/R조)화우미탁미정조(D조).채용협폐쌍측경총동맥연합저혈압법제비대서전뇌결혈재관주손상모형.D조우재관주즉각경경총정맥주사우미탁미정3 μg/kg부하제량,수후이3 μg· kg-1·h-1적속솔정맥수주지재관주2h.우재관주24 h시행신경공능결함평분(NDS평분),연후처사대서,취뇌조직,계수조망세포,계산세포조망솔,측정병이철(MDA)、초양화물기화매(SOD)화과양화경매(CAT)적수평.결과 여S조비교,I/R조화D조NDS평분、세포조망솔화MDA수평승고,SOD화CAT적수평강저(P<0.01);여I/R조비교,D조NDS평분、세포조망솔화MDA수평강저,SOD화CAT적수평승고(P<0.01).결론 우미탁미정통과억제양화응격반응감경대서전뇌결혈재관주손상.
Objective To evaluate the effects of dexmedetomidine on the oxidative stress responses during global cerebral ischemia-reperfusion (I/R) in rats.Methods Thirty-six male Sprague-Dawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =12 each) using a random number table:sham operation group (group S),global cerebral I/R group (group I/R) and dexmedetomidine group (group D).Global cerebral ischemia was induced by occlusion of bilateral common carotid arteries combined with hypotension (MAP maintained at 35-45 mmHg).In group D,dexmedetomidine was infused at a rate of 3 μg · kg-1 · h-1until 2 h of reperfusion after a loading dose of dexmedetomidine 3 μg/kg was intravenously injected immediately after onset of reperfusion.The neurological deficit score (NDS) was assessed at 24 h of reperfusion,the rats were then sacrificed,and their brains were immediately removed for determination of cell apoptosis and levels of malondialdehyde (MDA),superoxide dismutase (SOD) and catalase (CAT).Apoptotic rate was calculated.Results Compared with group S,NDS,apoptotic rate and MDA level were significantly increased,and SOD and CAT levels were decreased in I/R and D groups.Compared with group I/R,NDS,apoptotic rate and MDA level were significantly decreased,and SOD and CAT levels were increased in group D.Conclusion Dexmedetomidine attenuates global cerebral I/R injury through inhibiting the oxidative stress responses.